The single objective of this proposed research project is to understand the role of the sympathetic nervous system in the early pathophysiology of pulmonary insufficiency occurring with various kinds of regional and systemic trauma. Dogs will undergo unilateral or bilateral thoracic sympathectomy resulting in models with a single significant physiologic variable; namely, the absence of sympathetic nerves to one or both lungs. They will then be subjected to a low perfusion state (shock) or to central nervous system trauma. The shock subgroups will consist of dogs subjected to hemorrhagic, endotoxin, and cardiogenic shock. The central nervous system trauma subgroups will consist of dogs subjected to intracranial balloon inflation and CNS endotoxin infusion. During the early course of development of the lung injury, serial bronchospirometry, dynamic compliance, arterial blood gases, shunt fractions (Qs/Qt), and pulmonary and systemic hemodynamic determinations will be made on bilaterally denervated dogs. Xenon ventilation - perfusion scanning will be performed on unilaterally denervated animals to assess differential ventilatory and hemodynamic changes in the normally innervated and the denervated lung. Differential pulmonary hemodynamics will be measured in these unilaterally denervated dogs with bilateral pulmonary artery intraluminal flow probe-pressure catheters and a pulmonary wedge catheter. Any early physiologic differences between the normally innervated control dogs and the denervated models will be attributed to the activity of the pulmonary sympathetic nerves. If the sympathetic nervous system is important in post-traumatic pulmonary insufficiency, pharmacological manipulations with alpha-adrenergic blocking agents may prove beneficial in preventing or reversing the lung injury occurring in trauma.